reproductive patho

embryonic repro system

same in M & F until 8 wks
both have pair of undiff sex organs -- gonads
testosterone=testes
estrogen=ovaries

Pituitary Gland

source of all sex hormones

GH (growth hormone)

promotes protein anabolism, lipid mobilization, & catabolism
main effect on linear growth

ACTH (adrenocorticotropic hormone)

fosters growth of adrenal cortex
stims secretion of glucocorticoids

TSH (thyroid stimulating hormone)

stims syn and release of thyroid hormones & growth and fxn of thyroid

Gonadotropins

FSH (follicle stimulating hormone) and LH (lutenizing hormone) stim sex hormone secretion, repro organ growth, & repro processes

Somatotropin

released in diurnal pattern over 24 hrs
indirect effects via intermediary peptides (IGF)
direct effects on organs increases protein syn, cartilage growth, osteoblasts, & breakdown of fats

LH

site: ant. pituitary
target: W-ovarian follicle; M-Leydig cells
fxn: W-ovary dev., ovulation & progest produxn; M-spermatogenesis, testost produxn, testicular growth, & androgen produxn

FSH

site: ant. pituitary
target: W-ovarian follicle; M-Leydig cells
fxn: W-follicle maturation and estrogen produxn (ØFSH=Øreproduction);M-spermatogenesis

Prolactin

site: ant. pituitary
target: mammary glands
fxn: milk prodxn in W

Oxytocin

site: ant. pituitary
target: uterus
fxn: uterine contraction & milk ejection may impact sperm motility in M & anti-diuretic effects in M&W

Puberty

the transition between the juvenile state and the mature repro state when 2nd sex char dev and fertility is achieved

Puberty includes:

growth spurt growth of pubic & axil hair dev of 2ndary sex char (W-breasts & M-G&D of testes)

Thelarche

breast dev

Menarche

onset of menses

Pubarche

dev of pubic & axil hair, body odor, & acne

Adrenarche

↑ secretion of androgens from adrenal gland

Puberty in girls

8-9 y/o -- thelarche ∅ menses yet
2 yrs later -- menarche
complete in 5-7 yrs
apr. BW 48kg and need 16-24% fat

Puberty in boys

11-12 y/o -- adrenarche
complete in 5-7 yrs
apr. BW 48kg and need 16-24% fat

Tanner Staging

used to grade progress thru puberty
staged 1-5
1=Ø puberty
5=complete puberty
part of G&D check-up in adolescents

when is puberty complete?

W-ovary releases mature ova
M-ejaculation contains mature sperm

delayed puberty

lack of dev of 2ndary sex char after age 14 in girls or 15 in boys
happens in about 3% of children

causes of delayed puberty

genetic -- diseases like Turner's Syndrome and Klinefelter's Syndrome
anorexia or severe obesity
gonadal failure from trauma or infxn
HYPOthyroid
GH deficiency
pituitary adenoma
CNS defects of hypothalmus
marijuana use
chronic stress
medications (prednisone)

weight and delayed puberty

anorexia -- may be clinical anorexia or very active in sports and not enough body fat
obesity -- adipose tissue can ↑sex hormones in blood (cortisol?)

assessing delayed puberty

R/O hypothyroid and GH deficiency first

Precocious puberty

puberty onset before 8y/o in F and 9y/o in M

central precocious puberty

GnRH (gonadotropin releasing hormone) dependent -- CNS mediated
most common
just like normal pub but earlier age
caused by premature activation of GnRH generator in hypothalmus, resulting in premature secretion of estrogen or testosterone

causes of central precocious pub

idiopathic (most common in F)
CNS tumors (hamartoma, astrocytoma, glioma)
CNS disorders (↑ ICP, dev abnormalities, vascular disorders, hydrocephalus, head trauma, arachnoid/suprasellar cysts, infections, cranial surgery, irradiation, or chemo)
Long-term exposure to sex steroids???

peripheral precocious puberty

GnRH independent
doesn't start in CNS
triggered by peripheral ind. release of endogenous estrogens or androgens from adrenal gland or gonads
OR by exogenous exposure to sex steroids

causes of peripheral precocious pub

estrogen secreting ovarian tumors and follicular cysts
testicular (leydigs cells) tumors
severe, longterm hypothyroidism
congenital adrenal hyperplasia
exposure to exogenous sex steroids
rare conditions -- testotoxicosis or McCune-Albright syndrome

Testotoxicosis

present with early virilization but no rise in gonadotropins usually familial

McCune-Albright Syndrome (MAC)

causes breast dev w/o pubic hair and sometimes intermittant vaginal bleeding
classic triad:
--precocious sex dev
--hyperpigmented macules (café au lait lesions)
--fibrous bone dysplasia (may cause limp or fracture)

results of precocious pub

impaired adult height
psychosocial embarrassment
disturbed body image
scholastic underacheivement
↑ in high risk behaviors -- smoking, drinking, sex

eval of precocious pub

most important lab test is accurate spontaneous or GnRH stimulated LH level

LH levels in precocious pub

random of 0.1-0.3 or GnRH stim of 5-10 is suspicious/borderline
random of >0.3 or GnRH stim of >10 is definitely pubertal

levels in peripheral precocious pub

no LH increase, but high estrogen in F and high testosterone in M suppressed
FSH helpful indicator (also small testes in M indicate peripheral)

Menstrual Cycle Day 1

1st day of period

Menstrual Cycle Day 1-5

shedding lining slight in ↑ LH big ↑ in FSH to stim follicle dev in ovary

Menstrual Cycle Day 5-14

dom hormone=estrogen that peaks around 12-14 days
proliferation of endometrial lining (b/c est.)
feedback loop from ↑ est triggers LH surge (↑ LH)
ovulation occurs within 29-39 hrs of LH surge (around day 14)

Menstrual Cycle Day 15-26

dominated by progesterone (progesterone stops further egg dev)
secretory phase -- secretion of sugary substance on full uterine lining to feed blastocyst

Menstrual Cycle Day 26-28

corpus luteum dissolves = ↓ in estrogen & progesterone = menses = back to day 1

primary follicle

consists of primary oocyte surrounded by single layer of follicular cells
follicular cells are simple squamous cells that are converted to cuboidal cells by FSH and produce estrogen

zona pellucida

scattered spaces which enlarge and enclose oocyte
separate from inner follicular cells
also controlled by FSH
clear cell-free area

PMS

cluster of physical and psychological s/sx occurring 3-14 (average of 8) days before menses and relieved with onset of menses
unknown etiology but may be from serotonin

S/sx of PMS

vary greatly between women
psychological -- irritability, nervousness, depression, anxiety, ↓ concentration
GI -- food cravings, bloating, N/D, constipation
Neuromusc -- clumsiness, LBP, leg aches
gen -- wt. gain, insomnia, acne
repro -- swelling and tenderness of breast, pelvic congestions, ovarian pain, altered libido
progesterone makes body feel bad -- water retention, etc.

PMDD

like PMS but much more severe s/sx are bad enough to debilitate and cause social problems
needs medical tx (BC pills or SSRIs)

Normal menses

occurs every 24-32 days lasts 3-7 days average blood loss of 30cc

Amenorrhea

absence of menses for 6 mths

primary amenorrhea

absence of menses by 14y/o if 2ndary sex char present
OR by 16y/o regardless of presence of 2ndary char

secondary amenorrhea

cessation of menses for at least 6 mths in woman with established menstrual cycle
most common causes are pregnancy and PCOS

causes of 2ndary amenorrhea

pregnancy
PCOS
pituitary adenomas
endocrine disorders
excessive stress
wt. loss or just underwt. and/or excessive exercise (consider anorexia or bulemia in differential!)

Oligomenorrhea

infrequent menses (>35 days apart) or longer than 6-7 wks but less than 6 mths

menorrhagia

↑ amount and duration of flow that occurs at regular intervals

metrorrhagia

bleeding at more frequent intervals but not normally excessive (investigate and look at pill dosing)

menometrorrhagia

heavy, more frequent bleeding can cause anemia, fatigue, etc. (1cc of blood loss=0.5mg of Fe loss)

dysmenorrhea

painful menses

primary dysmenorrhea

menstrual pain NOT associated with pathology or abnormality
pain usually 1-2 days before menses and 1-2 days after start
dull, lower abd aching, cramping, may radiate to back, thighs, labia, or vagina r/t uterine contraction

secondary dysmenorrhea

menstrual pain r/t specific etiology
pt. hasn't always had pain, but starts suddenly and is bad -- worry b/c most likely pathologic commonly endometriosis, uterine fibroids, ovarian cysts (less commonly from IUD)

Age-related dysfunxnal bleeding

prepubescent -- sexual assault, trauma (foreign body in vagina)
adolescence -- anovulation (normal), irregular (normal to be irregular for about 2 yrs), sexual abuse, trauma
repro years -- pregnancy or PCOS
premenopause -- anovulation, malignancy
postmenopause -- malignancy (if pt. has not had bleeding for 1 yr and then starts suddenly, think endometrial cancer)

PCOS

problem with endocrine & repro systems
most common endo prob in US -- 8-10%
multisystem endocrine disorder

Patho of PCOS

↑ androgens (predominantly testosterone) cause ↑ in insulin secretion from pancreas (some ? about which comes 1st)
↑ insulin causes ↑ in androgen production = vicious cycle!
ALSO androgens= ↑testosterone in blood → body converts excess testosterone to estrogen→ too much estrogen= ↓ FSH & ↑ LH = many immature follicles, but none mature to ovulate

S/sx of too much androgen in PCOS

hirsutism (hair in upper lip, chin, chest, and abd)
acne
wt. gain

s/sx of too much insulin in PCOS

insulin resistance in the cells so ↑ risk for DM2
also ↑ angiotensin II and causes endothelial damage = ↑ CV risk factors
30% of PCOS pts will have DM2 by 30y/o

s/sx of too much estrogen in PCOS

↑ estrogen causes constant hyperplasia of the endometrium that is not shed → dysplasia=↑ risk for endometrial cancer

s/sx of too little FSH in PCOS

infertility b/c w/o FSH none of the follicles mature into funcxning ova → pearl necklace appearance in ovaries on U/S b/c all the immature follicles →oligo- or amenorrhea

etiology of PCOS

no clear answer
genetics is thought to play a big part
Stein-Leventhal syndrome
Cushing's syndrome
congenital adrenal hyperplasia
thyroid disease
androgen producing adrenal tumors
syndromes with hyperprolactinemia are also possibilities

Dx of PCOS

must have 2 of the 3 s/sx:
oligo- or anovulation
clinical or biochemical s/sx of androgenism
polycystic ovaries (pearl necklace on U/S)

Key S/Sx

Infertility b/c Ø ovulation (defining char)
pearl necklace appearance of ovaries
s/sx of androgens (hirsutism, acne, wt. gain)

Pregnancy and PCOS

if a PCOS pt can get pregnant, they are at ↑ risk for gestational diabetes and hypertension

s/sx of yeast vaginosis

white, thick, clumpy (cottage cheese) vaginal discharge
extreme pruritis (and redness)

causes of yeast vaginosis

alterations in host vaginal environment:
loss of lactobacillus
alterations in pH (pregnancy, stress, diabetes)
douching, fem hygiene sprays, detergents
antibiotics
hormonal changes (menopause?)
usually more in 16-24y/o

bacterial vaginosis

infection of vagina by many diff poss bacteria types -- not always STD results in inflammation of vagina

s/sx of bacterial vaginosis

vaginal discharge with:
--marked change in color (brown usually)
--sig ↑ amount
--foul odor
burning
erythema
presence of Clue cells
+ whiff test

Clue cells

show on stained slide of vaginal cultures when bacterial vaginosis is present

whiff test

when vaginal cultures on slide are exposed to KOH, will give off an odor if bacterial vaginosis is present = + whiff test

causes of bacterial vaginosis

strong antibacterial soaps
douches
foreign bodies
sperm (b/c basic pH)
strep and other bacteria

Trichomoniasis

protozoan infection
parasites feed off vaginal mucosa and produce copious, maloderous, greenish-yellow discharge

s/sx of trichomoniasis

greenish-yellow discharge (hallmark)
copious discharge
odor
strawberry appearance of cervix -- cervix is reddened and spotted

PID

inflammation of upper repro tract that involves uterus, fallopian tubes, or ovaries
systemic disorder!

endometritis

PID in uterus

salpingitis

PID in fallopian tubes

oophritis

PID in ovaries

causes of PID

bacterial infection of vagina/cervix moves upward
usually gonorrhea or chlamydia
SEX (esp. w/ mult partners)

s/sx of PID

lower abd pain
purulent discharge
pelvic tenderness
cervical motion tenderness
↑ WBC
fever
dysparenuria

cervical motion tenderness

severe pain with manipulation of cervix

dysparenuria

pain with sex

outcomes of PID

scar tissue in fallopian tubes can cause infertility
↑ risk for ectopic pregnancy

disorders of pelvic support

loss of support from pelvic floor muscles causes inability to maintain organs in correct position
usually 50-60y/o
familial tendancy
more in caucasians
↑ w/ mult pregnancies

cystocele

loss of pelvic support causes herniation of bladder into vagina -- bladder sags below uterus

s/sx of cystocele

bearing down sensation
cystitis
urinary frequency and urgency
stress incontinence
↑ risk for UTIs

rectocele

loss of pelvic support causes herniation of rectum into vagina

s/sx of rectocele

difficulty with defecation -- constipation
sensation of fullness in vagina

uterine prolapse

loss of pelvic support causes uterus to descend into vagina

s/sx of uterine prolapse

fullness or heaviness in vagina
back pain from tension on round ligaments
bladder pain

staging of uterine prolapse

staged 1-4
1=little drooping -- may not even notice on pelvic exam
4=uterus is out of vagina

Functional ovarian cysts

follicular or corpus luteum

Follicular Functional Ovarian Cysts

results from occlusion of the duct of the follicle and dom follicle fails to rupture
fluids get trapped and is very painful until it ruptures
usually resolves on it's own
most common and results from NORMAL funxn

corpus luteum functional ovarian cysts

bleeding into corpus luteum
more painful than follicular
rupture may cause bleeding or irregular periods
pain usually on one side w/ bleeding

dermoid ovarian cysts

ovarian teratomas -- germ cells in primary oocyte go haywire and get other types of tissue growing on the ovary -- skin, hair, seb & sweat glands, muscle, or bone
precancerous but usually benign
can be bi- or unilateral

outcomes of dermoid ovarian cysts

can cause ovarian torsion
large ones can rupture and cause adhesions, pain
must be removed b/c can become malignant

Leiomyomas (uterine fibroids)

benign tumors from overgrowth of normal tissue

types of leiomyomas

based on location:
submucosal
intramural
subserous

submucosal leiomyomas

inside uterus

intramural leiomyomas

in muscle of uterus

subserous leiomyomas

attached to outside of uterus

s/sx of leiomyomas

may be assymptomatic
s/sx vary with location
--urinary urgency, frequency, or dysuria if near bladder
--constipation, abd pain, rectal pressure if near rectum
may have excessive bleeding or cramping
menorrhea, menometrorrhea, or 2ndary dysmenorrhea

outcomes of leiomyomas

generally slow growing and benign problem, but estrogen can increase growth such as with pregnancy or BC pills
if they get too big for blood supply, can become necrotic and ulcerative

endometriosis

proliferation of endometrial tissue outside the uterus that is responsive to normal menstrual cycle unknown cause -- possible genetic

s/sx of endometriosis

classic triad:
--dysmenorrhea
--dysparenuria
--infertility (one of the leading causes)
(infertility and dysparenuria from cells triggering inflammatory process and causing adhesions/scar tissue)
cyclic pain during mth as cells respond to estrogen levels in mid cycle
dyschezia (pain with defecation)

chocolate cysts

ectopic endometriosis implants in the ovary
may form cysts with old blood cells
get together and form a capsule → then respond to estrogen & bleed → blood gets trapped and can get infected when blood gets old
rupture may cause peritonitis and adhesions

s/sx of chocolate cysts

dark brown bleeding and severe pain

endometrial cancer

most common repro cancer
more in caucasians, but AA die from it more
generally adenocarcinoma

risk factors for endometrial cancer

obesity
high fat diet
infertility or nullparous
caucasian over 40y/o
family hx
diabetes
hx of breast or ovarian cancer
HRT with just estrogen b/c causes endometrial hyperplasia but there is no shedding = dysplasia
early menarche and/or late menopause

s/sx of endometrial cancer

post-menopausal bleeding

ovarian cancer

2nd most common repro cancer
highest mortality rate
arises from uterine epithelium

s/sx of ovarian cancer

almost none! so very hard to find and dx
vague
GI -- bloating, N/V, constipation, dyspepsia, ascites
difficult to impossible to feel on bimanual exam but try anyway
usually found after mets=poor prognosis

risk factors for ovarian cancer

family hx of ovarian, breast, uterine, pancreatic, or colon cancer
may result from trauma to ovary (every time an egg is released the ovary is traumatized and there is an inflammatory response)
use of infertility drugs w/o pregnancy
HRT may ↑ risk but BC pills ↓ risk
early menarche and/or late menopause

oncogenes in ovarian cancer

HER2+
RAS
almost all from mutation of the P53 tumor suppressor genes

breast cancer

most common F cancer
incidence ↑ with age
early detection ↓ mortality, but 2nd only to lung cancer in death rate

risk factors for breast cancer

age
personal or family hx (↑ risk 2-3x)
hx of atypical hyperplasia of breasts
↑breast density
long menstrual hx
obesity after menopause
recent use of BC pills or post-meno HRT (est & pro)
nullparous or children after 30y/o
1+ alcoholic drinks/day
BRCA1 or BRCA2 mutations
radiation exposure

decreasing risk for breast cancer

tamoxifen
physical activity and healthy wt
early pregnancy

oncogenes in breast cancer

BRCA1 & 2
p53 tumor suppressor gene mutations
ERBB2 oncogenes -- HER1, 2, & 3=more aggressive cancer mutations with estrogen receptors on cancers make them estrogen dependent

types of breast cancer

ductal carcinoma
lobular carcinoma

ductal carcinoma breast cancer

cancer arising from collecting ducts
easier to find b/c more toward surface
ductal infiltrating carcinoma is most common type of breast cancer
usually found in upper, outer quadrant of breast

lobular carcinoma breast cancer

arises from terminal lobules
can grow more and spread out with less formation of dense solid tumors so harder to detect

breast cancer nodules

firm, fixed, and painless

s/sx of breast cancer

painless lump
dimpling
discoloration
inverted nipple
discharge from nipple
chest pain
ulceration
edema
peau d' orange appearance
change in size or shape of breast
mets

sentinal node biopsy with breast cancer

biopsy of closest lymph node to the cancer site to check for mets
helps determine need for aggressive tx

cervical cancer

direct relationship to HPV infection b/c it causes an oncogenic mutation
easy to tx if caught early -- PAP smear!
Almost impossible to tx in late stages

risk factors for cervical cancer

HPV infection
hx of sex before 16 y/o
mult sex partners
poor nutrition
smoking
+family hx
DES in utero -- DES was a drug that was given to women who had miscarriages to help maintain the pregnancy -- worked, but caused cervical abnormalities in the child

phimosis

foreskin cannot be retracted over glans
foreskin is swollen, painful, irritated, and can block the urethra or move further up the penis
only in uncircumcized men

causes of phimosis

poor hygiene and chronic infection like DM2 (can be a presenting s/sx of DM2 so check for it)

paraphimosis

foreskin is retracted and cannot be replaced back over the glans due to inflammation, pain, etc.
only in uncircumcized men
Medical Emergency! b/c can cut off blood supply
May need surgery

causes of paraphimosis

poor hygiene and chronic infection like DM2 (can be a presenting s/sx of DM2 so check for it)

Peyronie's Disease

progressive fibrosis of the sheath around the corpora cavernosa of penis
causes painful bent erections
usually in men 40-60y/o
unknown cause
variable progression and severity

priapism

involuntary, prolonged, abnormal, painful erection lasting longer than 4 hours
can result in ischemia of penis so is a medical emergency

age and priapism

boys 10-12 b/c pulses of testosterone
20-50 idiopathic
older than 50 usually related to ED tx

risk factors for priapism

illicit drug use -- marijuana & cocaine
spinal cord trauma -- less neuro control
use of ED drugs

balanitis

inflammation of glans of penis
can happen regardless of circumcision status
generally benign but recurrence can cause scarring around the urethra
caused by poor hygiene and DM2
tx with antibiotics

Pearly penile papules

ring of white dots at the base of the glans
idiopathic & benign
no tx necessary
not related to sexual hx

varicocele

varicosities of veins supplying testes -- blood pools in veins around spermatic cord
can decrease sperm count
15-35y/o
surgery is only tx

s/sx of varicocele

feels like bag of worms
heavy, achy pain or none at all

hydrocele

fluid accumulation w/in tunica vaginalis -- tube in infant to allow testes to descend doesn't close off and fluid from abd gets in can occur w/ all ages --
adults 2ndary to trauma or infection
may require surgical aspiration of fluid
not associated with infertility

s/sx of hydrocele

extremely swollen scrotum
feels like a water balloon
non-tender b/c no infection
should transilluminate fluid when light is shined on scrotum

spermatocele

cyst containing sperm at end of epidydimis
small lump on top of testicle that is generally soft and painless
order U/S to r/o testicular cancer
not associated with infertility

cryptorchidism

one or both testes fail to descend
requires surgery if don't descend by age 1
associated with inferility if not corrected
always ↑risk of testicular cancer

testicular torsion

twisting of spermatic cord
abrupt and often associated with trauma
medical emergency b/c twisting can cut off blood supply

s/sx of testicular torsion

severe pain radiating to groin
anxiety
n/v
enlarged testicle (not always)

epididymitis

inflammation of epididymis -- usually r/t infection
19-35 y/o -- usually gonorrhea or chlamydia
50+ y/o -- r/t prostate enlargement

risk factors for epididymitis

uncircumcized
mult sex partners
recent cath
rare -- amiodarone induced

s/sx of epididymitis

blood in semen
discharge
fever
painful lump
pain with ejaculation and/or urination
swelling

orchitis

acute inflammation of the testes
usually occurs with epididymitis
usually from gonorrhea or chlamydia OR mumps

s/sx of orchitis

(like epididymitis)
blood in semen
discharge
fever
painful lump
pain with ejaculation and/or urination
swelling
+ tender, enlarged testicle

testicular cancer

most common solid tumor in young men
15-35 y/o
can be benign or malignant
can be palpated so teach self-exams
mets quickly to lungs and brain=poor prognosis
surgically remove effected teste
most come from germ cells that create sperm

risk factors for testicular cancer

AA
+family hx

s/sx of testicular cancer

hard mass that doesn't move -- feels like frozen pea or grape
painless enlargement of the testes
feeling of heaviness in lower abd

HPV

mult strains -- some cause genital worts & some cause nothing
6 strains have been proven to cause cervical cancer
can cause oral, penile or anorectal cancer
CAN be spread even w/ a condom
no tx/cure
variable course
drugs to manage erruptions

genital herpes infection

HSV-2 virus
replicates in skin (lives in sacral dorsal root ganglia)
can be dormant for years
not exclusive to genital area
CAN be spread even w/ a condom
reactivated by stress, illness, extreme temp changes, or immunosuppression

s/sx of genital herpes

tingling and pruitits with erruption
vesicles that ulcerate
pain
dysparenuria
fever
headache
muscleaches
lymphadenopathy
when 1st infected usually experience flu-like s/sx

chlamydia

bacterial infection transmitted by oral, vaginal, or anal contact
curable with antibiotics
most common STD
untreated infection can lead to PID and infertility
preventable with condoms

s/sx of chlamydia

usually no s/sx in women
urinary frequency
dysuria
vaginal or penile discharge (penile leakage just drips constantly)

gonorrhea

bacterial infection that can go thru bloodstream and cause systemic effects especially in the joints -- #1 cause of infective arthritis
can be passed to infants during birth and cause gonorrheal conjunctivitis that can lead to blindness -- must have c-section to avoid
can cause PID and infertility
can be stopped with condoms
getting harder to tx outpt b/c resistance -- only Rocephin IM now

s/sx of gonorrhea

2-7 days after exposure: purulent discharge from vagina or penis
dysuria

syphilis

4 stages:
primary
2ndary
latent
tertiary

primary syphilis

non-painful (unique) chancre sores at site of infection (genitals, mouth, etc.)
occurs 3-4 wks after transmission and lasts for 5 wks
contagious at this pt
best time to tx

2ndary syphilis

occurs about 6 wks after resolve of chancre sores
Nickle and Dime rash on palms (rare!) and may have some central clearing
most contagious stage
rash spontaneously heals in about 6 wks
still treatable

latent syphilis

can be latent for 1 yr or whole life but it's still in the body and can be reactivated if immunosuppressed

tertiary syphilis

systemic, neurological s/sx develop -- dementia, ↓ LOC, memory loss
run RPR (reactive plasma reagent) to test for syphilis with all new dementia pts
lesions on bones, skin, and soft tissue -- bones become brittle
CV complications -- inflammation in BVs, heart, valves, and ↑ risk for aortic aneurysm
can still be treated but s/sx are not reversible

reproductive patho

Nursing 655 with Herman at University of Louisville

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